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ECG-In-The-Athlete.Pdf Electrocardiogram in the Athlete Joint Session ISE-FIAI-SOLAECE-SIAC ICE 2015 Comandatuba, Bahia, Brazil Martín Ibarrola MD, FAHA Centro Cardiovascular BV Director of Medical Department of Sports Rugby and Hockey. Club Regatas de Bella Vista Argentina Pre-participation screening can prevent sudden cardiac death in the athletes ▪Medical history: ➢Personal history. ➢Family history ➢Physical examination ▪ ECG changes that would be considered abnormal in the untrained population may develop in trained athletes as a physiologic and benign consequence of the heart's adaptation to exercise. Italian program ▪ Young competitive athletes aged 12 to 35 years are included. ▪ 2 consecutive screening periods (1982-1992and1993-2004) in Italian program. The number of competitive athletes aged 12 to 35 years in the Veneto region from 1982 to 2004 was 42 386 athletes Interpretation of ECG in athlete’s ▪ 12-lead ECG in the athlete: physiological versus pathological abnormalities. Review. Br J Sports Med 2009. Corrado D. MD; et al. ▪ Recommendations for interpretation of 12-lead electrocardiogram in the athlete. ESC REPORT. European Heart Journal 2010. Corrado D. MD; et al. ▪ Interpretation of the Electrocardiogram of Young Athletes. Special Report. Uberoi A. MD; et al. Circulation 2011 ▪ Electrocardiographic interpretation in athletes: the ‘Seattle Criteria’. Br J Sports Med 2013. Drezner J A; et al. Refinement of the European Society of Cardiology (ESC) criteria ▪ Improving the interpretation of the athlete’s electrocardiogram. EDITORIAL. Corrado D. el al. European Heart Journal 2013 European Society of Cardiology (ESC) classification of ECG abnormalities in athletes Recommendations for interpretation of 12-lead electrocardiogram in the athlete Group 1: common and Group 2: uncommon and training-related ECG training-unrelated ECG changes (>80%) changes (<5%) ▪ Sinus bradycardia ▪ T-wave inversion ▪ First-degree AV block ▪ ST-segment depression ▪ Incomplete RBBB ▪ Pathological Q-waves ▪ Early repolarization ▪ Left atrial enlargement ▪ Left-axis deviation/left anterior ▪ Isolated QRS voltage hemiblock criteria for left ventricular ▪ Right-axis deviation/left posterior hypertrophy hemiblock ▪ Right ventricular hypertrophy ▪ Ventricular pre-excitation ▪ Complete LBBB or RBBB ▪ Long- or short-QT interval ▪ Brugada-like early repolarization Domenico Corrado, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. European Heart Journal (2010) 31, 243–259 The ‘Seattle Criteria’: Electrocardiographic interpretation in athletes (1) Normal ECG findings in athletes Abnormal ECG findings in athletes (1) T-wave inversion >1 mm in depth in two or more leads V2–V6, II and aVF, or I and 1. Sinus bradycardia (≥ 30 bpm) aVL (excludes III, aVR and V1) 2. Sinus arrhythmia ST segment depression ≥0.5 mm in depth in two or more leads Pathologic Q waves >3 mm in depth or >40 ms in duration in two or more leads 3. Ectopic atrial rhythm (except for III and aVR) 4. Junctional escape rhythm Complete left bundle branch block QRS ≥120 ms, predominantly negative QRS complex in lead V1 (QS or rS), and upright monophasic R wave in leads I and V6 5. 1° AV block (PR interval > 200 ms) Intraventricular conduction delay. Any QRS duration ≥140 ms 6. Mobitz Type I (Wenckebach) 2° AV block Left axis deviation −30° to −90° Left atrial enlargement Prolonged P wave duration of >120 ms in leads I or II with 7. Incomplete RBBB negative portion of the P wave ≥1 mm in ventricular hypedepth and ≥40 ms in duration 8. Isolated QRS voltage criteria for LVH in lead V1 Right hipertrophy pattern ▸ Except: QRS voltage criteria for LVH occurring R−V1+S−V5>10.5 mm AND right axis deviation >120° with Ventricular pre-excitation PR interval <120 ms with a delta wave (slurred upstroke in any non-voltage criteria for LVH such as left the QRS complex) and wide QRS (>120 ms) Long QT interval* atrial QTc≥470 ms (male) enlargement, left axis deviation, ST segment QTc≥480 ms (female) depression, T-wave inversion or pathological QTc≥500 ms (marked QT prolongation) Short QT interval* Q waves (1) And the Right blundle branch block QRS >120msQTc≤320 ms and <139 ms? 9. Early repolarisation (ST elevation, J-point Brugada-like ECG pattern High take-off and downsloping ST segment elevation followed by a negative T wave in ≥2 leads in V1–V3 elevation, J-waves Profound sinus bradycardia <30 BPM or sinus pauses ≥ 3 s or terminal QRS slurring) Atrial tachyarrhythmias Supraventricular tachycardia, atrial-fibrillation, atrial-flutter 10. Convex (‘domed’) ST segment elevation Premature ventricular contractions ≥2 PVCs per 10 s tracing combined with T-wave inversion in leads V1–V4 Ventricular arrhythmias Couplets, triplets and non-sustained ventricular in black/African athletes tachycardia Drezner JA, Ackerman MJ, Anderson J, et al. Br J Sports Med 2013;47:122–124. (1) In Seattle Criteria normal o abnormal findings in athletes ▪ The author have omitted mention of Complete Right bundle branch block QRS ≥120 ms and < 140 ms. I send to author a letter about this point about the implication of this and respond by mail “Dear Dr. Ibarrola, Thank you for the note. I appreciate your comments regarding RBBB. I think the pre-test probability that complete RBBB represents disease in most asymptomatic athlete populations is very low. Thus, in most settings I don’t think RBBB has a high positive predictive value and will not be a good distinguisher of disease. You bring up an important point that was not addressed in the Seattle summit papers -- that RBBB in countries with a high prevalence of Chagas disease should be considered abnormal. This will be considered in any future revisions to the criteria.” Response by Jonathan Drezner, MD This omitting affected papers compared to ESC recommendation compared with the Seattle Criteria. The complete RBBB have present in 1% of athletes (Pelliccia et al. EHJ 2007) but is normal o abnormal findings in athletes? In countries with Chagas disease, if reasonable? Affected this the support of better false positive in comparative paper’s? Interpretation of the athlete’s electrocardiogram Domenico Corrado et al. Improving the interpretation of the athlete’s Electrocardiogram. European Heart Journal (2013) 34, 3606–3609 Electrocardiographic Findings in athletes normal variants GROUP 1 Athletes normal variants Increased vagal tone Changes of increased cavity dimensions and wall thickness Sinus bradycardia (≥ 30 bpm). P wave must have a normal axis in the frontal plane (0–90°s) Male 27 years old. Rugby player. Sinus bradycardia 41 bpm Sinus arrhythmia Female 14 years old. Voley. 64 BPM. Sinus arrythmia Ectopic atrial rhythm: P waves are present but are a different morphology compared to the sinus P wave, negative in the inferior leads (II, III and aVF) Junctional escape rhythm or nodal rhythm Male 15 years old. Rugby player. Asyntomatic. Nodal rhytmin First-degree AV block: PR interval is prolonged (>200 ms) 27 years old 23 years old 2011 2015 Male, Rugby player, asymtomatic with BAV 1er grade 0,24 ms Second-degree AV block: Mobitz type I (Wenckebach) Male 32 years old. Asymtomatic. Intensive Spining. Early repolarization: concave ST segment elevation in the precordial leads. New definitions of Early Repolarization Types 1, 3 and 5 all have an elevated ST amplitude ≥0.1 mV with or without a notch or slur while Types 2 and 4 have the peak of a notch or onset of a slur ≥0.1 mV but without ST elevation. Peter W. Macfarlane. J wave patterns — morphology, prevalence and nomenclature. J Electrocardiol. 2013 Nov-Dec;46(6):505-9 Early repolarization Isolated QRS voltage criteria for LVH for Sokolow- Lyon criterion Incomplete right bundle branch block Male 17 years. IRBBB Abnormal electrocardiographic findings in athletes GROUP 2 Mimics incomplete Right bundle branch block ▪ Abnormal IRBBB pattern associated with other ECG abnormalities, T wave inversion involving the mid-precordial leads to V1–V3, prolonged S wave upstrokein individuals >14 years of age, low limb-lead voltages, prolonged S wave upstroke and/or premature ventricular beats with a left bundle branch block (LBBB) morphology and Epsilon waves in ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY ▪ Brugada-ECG pattern, which is characterized by a high take-off and downsloping ST segment elevation followed by a negative T wave in ≥2 leads in V1–V3. ‘J wave’ reflects early repolarisation with J point elevation and a high take-off with downsloping ST segment followed by a negative T wave Criteria for diagnosis of ARVC/D 1. Family history Major ▪ Familial disease confirmed at necropsy or surgery. Minor ▪ Family history of premature sudden death (<35 years of age) due to suspected ARVC/D. ▪ Family history (clinical diagnosis based on present criteria). 2. ECG depolarization/conduction abnormalities Major ▪ Epsilon waves or localized prolongation (>110 ms) of QRS complex in right precordial leads (V1-V3). Minor ▪ Late potentials on signal-averaged ECG. 3. ECG repolarization abnormalities ▪ Minor ▪ Inverted T waves in right precordial leads (V2 and V3) in people >12 years of age and in absence of right bundle branch block. 4. Arrhythmias Minor ▪ Sustained or nonsustained left bundle branch block-type ventricular tachycardia documented on ECG or Holter monitoring or during exercise testing. ▪ Frequent ventricular extrasystoles (>1000/24 h on Holter monitoring). 5. Global or regional dysfunction and structural alterations* Major ▪ Severe dilatation and reduction of RV ejection fraction with no or mild LV involvement. ▪ Localized RV aneurysms (akinetic or dyskinetic areas with diastolic bulgings). Severe segmental dilatation of RV. Minor ▪ Mild global RV dilatation or ejection fraction reduction with normal LV. ▪ Mild segmental dilatation of RV. ▪ Regional RV hypokinesia. 6. Tissue characteristics of walls ▪ Major ▪ Fibro-fatty replacement of myocardium on endomyocardial biopsy. ▪ * Detected by echocardiography, angiography, magnetic resonance imaging, or radionuclide scintigraphy. Modified from McKenna et al. BRUGADA PATTERN TYPE-1 TYPE-2 ▪ The differential diagnosis of Type-2 Brugada pattern and electrocardiogram of athletes Chevallier S, et al.
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